A variety of sleep disturbances has been described in epileptics. The sequencing of sleep stages may be atypical, rapid-eye-movement (REM) sleep may be disrupted, and sleep spindles are often irregular or suppressed. Seizures and interictal discharges are common during sleep, and recent findings indicated that sleep disturbances appear early and may contribute to the development of experimental seizure disorders. There is also evidence that sleep deprivation can facilitate seizures by exacerbating existing sleep disturbances. Conversely, an attenuation of seizures has been generally associated with the REM state and, more recently, with normalization of sensorimotor sleep spindles. REM sleep and sleep spindles are accompanied by various forms of motor inhibition. Further, a variety of experimental procedures enhancing motor inhibition both facilitated normal sleep and reduced seizures. Seizure activation during sleep may therefore arise from pathological sleep processes associated with enhanced motor excitability. The proposed studies will examine this hypothesis using the amygdaloid kindling model of epilepsy in cats. After-discharge and major motor seizure thresholds will be evaluated at different points during the sleep process in relation to changes in motor excitability. The latter will be indexed by the presence or absence of phasic motor activity and of rhythmic sensorimotor EEG patterns associated with motionlessness. Testing will be conducted during light slow-wave sleep (SWS), deep SWS, REM sleep and transitional periods between SWS and REM. We will also examine the effects of SWS and REM sleep deprivation on motor activity levels, sensorimotor EEG patterns and seizure thresholds. A physiological model of sleep disturbance will be produced with basal forebrain lesions, which have been shown to suppress REM and SWS at different post-lesion intervals. Since a suppression of SWS and REM sleep occurs with the development of kindled foci, both types of sleep loss are expected to facilitate seizure thresholds. In addition, reduced seizure thresholds should be correlated throughout with EEG and motor excitability changes.